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抗PcrV抗体与抗生素联合使用减少铜绿假单胞菌适应性产生
An Anti-PrcV Antibody Combined with Antibiotic Therapy Reduces the Generation of Antibiotic-resistant Pseudomonas aeruginosa Strains
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DOI:
作者:
何虹1,#,朱燕凤2,#,王琴2,#,刘洁2,宋元林2, 侯东妮2,*,曾玫3,*
Hong He1,#, Yan-feng Zhu2,#, Qin Wang2,#, Jie Liu2, Yuan-lin Song2, Dong-ni Hou2,*, Mei Zeng3,*
作者单位:
1复旦大学附属肿瘤医院麻醉科(上海,200032);2复旦大学附属中山医院呼吸科(上海,200032);3复旦大学附属儿科医院感染传染科(上海,201102)
1 Department of Anesthesiology, Cancer Hospital,Fudan University,Shanghai,200032,China; 2 Department of Pulmonary Medicine,Zhongshan Hospital,Fudan University,Shanghai,200032,China; 3 Department of Infectious Disease,Children's Hospital,Fudan University,Shanghai,201102,China
关键词:
铜绿假单胞菌;免疫治疗;腹腔感染;抗体;抗生素耐药
Pseudomonas aeruginosa; Immune therapy; Peritoneal infection; Antibody; Antibiotic resistance
摘要:
目的:既往抗生素治疗是产生细菌耐药,包括铜绿假单胞菌耐药菌株的独立危险因素,本研究旨在观察抗生素基础上联合使用抗铜绿假单孢菌PcrV单克隆抗体Mab166对细菌耐药性的影响。 方法:本研究使用腹腔内注射铜绿假单胞菌建立小鼠腹腔感染模型,分别用PrcV抗体Mab166、不同种类抗生素,或二者联合使用,观察不同处理方式对铜绿假单胞菌感染的保护作用,并用肉汤稀释法测定腹水中细菌对相应抗生素的敏感性。 结果:高剂量的Mab166治疗组能够显著延长PA腹膜炎模型小鼠的生存时间,但不能改善存活率。单用Mab166治疗可减少相同抗生素浓度下细菌生长的OD值以及抗生素的MIC值。经头孢他啶治疗后,诱导出了耐药PA菌株,在头孢他啶浓度为513mg/L的培养基中仍有细菌生长。而头孢他啶联用Mab166时腹水培养OD值及MIC明显降低,可减少耐药菌株的产生。妥布霉素和哌拉西林/他唑巴坦联合Mab166治疗未出现耐药菌株。 结论:抗PcrV抗体Mab166与抗生素治疗联合能够提高抗生素敏感性,且能够降低抗生素诱导产生的耐药,在临床治疗中有较高的应用价值。
Objectives Previous antimicrobial treatment is an independent risk factor for antimicrobial resistance, and also generation of antibiotic-resistant Pseudonoma aeruginosa (PA) strains. This study is designed to investigate if antibiotic treatment combined with monoclonal antibody—Mab166, which binds PrcV protein of PA, could reduce generation of drug-induced antibiotic resistance. Methods Mice model was established by intraperitoneal injection of PA103 strain. Mice were treated using antibiotics (ceftazidime, tobramycin or piperacillin/tazobactam), anti-PrcV antibody Mab166, or antibiotics and Mab166. Survival rate, rectal temperature and antimicrobial susceptibility were used to compare implications of different therapies. Results High dose of Mab166 treatment significantly prolonged survival time of PA infected mice, however, overall survival rate was not improved. Additionally, Mab166 could reduce OD value of peritoneal bacteria culture that contains different types of antibiotics at distinct concentrations, suggesting increased susceptibility of bacteria. After treatment with ceftazidime, antibiotic-resistant PA strains were induced, which could proliferate in medium with high concentration of ceftazidime (513mg/L). However, when Mab166 was used in addition to ceftazidime, the OD values and MIC largely decreased, indicating a reduction in PA resistance. No resistant strains were found in mice received Mab166 in combination with tobramycin or piperacillin/tazobactam. Conclusion Anti-PrcV antibody Mab166 combined with antibiotic therapy increases antibiotic susceptibility of PA and reduces the generation of drug-induced resistant strains, suggesting potential benefit of anti-PrcV antibody as an immunotherapy in clinical treatment of PA infection.
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